Barry Seemungal (PhD FRCP) is a neurologist who researches the brain mechanisms of vestibular function and dysfunction, with a focus on vestibular cognition. He was born and raised in Trinidad, West Indies, studied medicine in Cardiff and initially trained as an endocrinologist in Oxford and then as a neurologist in London, completing a PhD in vestibular neurosciences ('The Mechanisms and Loci of Vestibular Perception') at the Institute of Neurology, Queen Square, London. Dr Seemungal has received research funding from the Academy of Medical Sciences and Health Foundation Clinician Scientist Fellowship Programme, the Medical Research Council UK, the EPSRC, Imperial College Charities and the Friends of St Mary's.
SELECTED RECENT PUBLICATIONS
Kaski D, Quadir S, Nigmatullina Y, Malhotra PA, Bronstein AM, Seemungal BM. Temporoparietal encoding of space and time during vestibular-guided orientation. Brain. 2016 Feb;139(Pt 2):392-403. [OPEN ACCESS].
Yousif N, Bhatt H, Bain PG, Nandi D, Seemungal BM. The effect of pedunculopontine nucleus deep brain stimulation on postural sway and vestibular perception. Eur J Neurol. 2016 Mar;23(3):668-70. [OPEN ACCESS]
Nigmatullina Y, Hellyer PJ, Nachev P, Sharp DJ, Seemungal BM. The neuroanatomical correlates of training-related perceptuo-reflex uncoupling in dancers. Cereb Cortex. 2015;25:554-62. [OPEN ACCESS].
Seemungal BM, Guzman-Lopez J, Arshad Q, Schultz SR, Walsh V, Yousif N. Vestibular activation differentially modulates human early visual cortex and V5/MT excitability and response entropy. Cereb Cortex. 2013 Jan;23(1):12-9. [OPEN ACCESS].
Seemungal BM. The cognitive neurology of the vestibular system. Curr Opin Neurol. 2014 Feb;27(1):125-32.
(Consensus paper) Lempert T, Olesen J, Furman J, Waterston J, Seemungal B, Carey J, Bisdorff A, Versino M, Evers S, Newman-Toker D. Vestibular migraine: diagnostic criteria. J Vestib Res. 2012;22(4):167-72. [OPEN ACCESS].
TEACHING & DEVELOPING GUIDELINES
Online learning tools - NHS ENGLAND. See London Strategic Clinical Network Website:
Guidance for clinicians who are non-experts in vertigo -
Taken from: Seemungal. Curr Op in Neurology. 2007.
Member of the Barany Society involved in the working group that published the first classification for vestibular migraine.
Registered expert on the European Research and Innovation database.
Expert review of the United Kingdom ‘NICE’ guidelines for vertigo & dizziness.
Chaired a European conference on Brain Plasticity in the Vestibular system (‘FENS’ Satellite conference – 2014).
Association of British Neurologists Acute Neurology Advisory Group member.
This includes masterclasses on managing dizziness at the Royal College of Physicians, at BMJ Masterclasses in India and at the 1st and 2nd European Academy of Neurology (EAN) meetings in Berlin (2015) and Copenhagen (2016).
Participates in the Trust acute neurology rota. Provides an acute vertigo service with colleagues (Prof Adolfo Bronstein) at Imperial Healthcare NHS Trust. Together, they provide an acute vertigo service to the Trust A&E's, Hyperacute Stroke Unit at Charing Cross and the Major Trauma Unit at St Mary’s Hospital.
The Brain Mechanisms and Loci of Human Vestibular Perception.
A particular theme of our research is the uncoupling of perception and reflex function in the vestibular and ocular-motor system. We have published a brain imaging study which showed that the vestibular cerebellar grey matter is key in modulating sensations of dizziness separate from vestibular ocular reflex responses. In addition, we have demonstrated an extensive white matter cortical network involved in mediating vertigo sensation. These findings in healthy humans were corroborated in a recent human lesion study in which the loci of vestibular perception were probed in acute stroke patients.
Vestibular Mechanisms and Human Brain Diseases.
We are now extending our techniques into understanding the higher-order vestibular contributions to neurodegenerative diseases such as Parkinson's Disease. Our recent work aims to understand the brain mechanisms underlying effects upon balance function with novel deep brain stimulation targets in Parkinson's patients.
The Mechanisms of Brain Plasticity and Treating Balance Disorders.
BRAIN PLASTICITY OF THE VESTIBULAR AND OCULAR MOTOR SYSTEMS. FENS SATELLITE MEETING (3-4Th July, 2014, Como, Italy)
This meeting focused on the brain plasticity in the vestibular and ocular motor systems. The speakers were from a variety of backgrounds including electrophysiology, pharmacology, optogenetics, computational modelling, scientific studies of human brain function as well as clinical studies. (Conference webpage).
BRAIN PLASTICITY IN HEALTH AND DISEASE
Environmental change or change in our ‘internal milieu’ due to disease, poses a challenge to the survival of the individual. Brain plasticity is a key contributor to our remarkable capacity to adapt to external or internal change. Such plasticity is utilised in rehabilitation regimens be they physical or cognitive behavioural therapy. Occasionally brain plasticity may go wrong and cause symptoms. In my clinic a common if under-recognised condition called Visually-Induced Dizziness, may be due to such brain plasticity gone wrong.
We use the well characterised vestibular and ocular motor systems to measure and understand brain mechanisms of plasticity. By understanding brain plasticity better we aim to improve treatments for brain diseases that can be affected by the brain processes of plasticity.
LAB TO BEDSIDE
How the dancer’s brain adapts to repeated pirouetting.
We recently demonstrated the brain adaptation in dancers that enable them to suppress dizziness following a pirouette. We found that the vestibular cerebellum grey matter changed in line with the amount of training dancers did. This publication was covered in the media locally and internationally (see news). We are translating these findings in developing a new therapy for chronic dizzy patients. Together with colleagues from Kings College London and University College London, we are developing a dance-based treatment for patients with chronic dizziness. We also aim to combine this therapy with medication to speed recovery from chronic dizziness. We will also apply a modified version of this therapy to other neurological conditions such as rehabilitation for stroke patients.
How the brain adapts to continuous retinal image motion.
Do you remember spinning around till you fell in the school playground? An important response to continuous on-the-spot turning is a transient eye oscillation called nystagmus. This causes retinal image motion of the visual world and an unpleasant perception of visual world motion. Imagine if your eye was continuously oscillating? In this case you might see the visual world move continuously. Most people born with a nystagmus (congenital nystagmus) and some people who acquire a nystagmus as adults, fortunately do not see the world as moving but see it as still. This comes about because of brain changes that compensate for their continuous eye movement. At present we have no idea what brain regions or precisely what mechanisms might be important for this adaptation. This knowledge would be important for developing new treatments for the many patients (e.g. from multiple sclerosis, stroke, neurodegeneration) who acquire nystagmus in adulthood and have a continuous sensation of visual world motion.
The mechanisms by which congenital nystagmus subjects see the visual world as still have been debated for many decades but there are two competing hypotheses: (1) visual cortex spatial updating of eye position (2) suppression of visual motion cortical activity. Some proponents of the spatial updating theory have upheld that this can be the ONLY mechanism to explain visual perceptual stability in congenital nystagmus. A major reason for this debate is that only behavioural data have been obtained rather than direct measurements of brain functioning. Using brain stimulation responses we have been able to directly probe the brain mechanisms involved in visual perceptual stability in congenital nystagmus. Our data (manuscript in preparation) show that in congenital nystagmus, there are two mechanisms at play which may be utilised independently or together, in visual motion cortex : (i) updating of eye position to account for the change in the visual image due to the eye oscillation (ii) phasic suppression of cortical excitability – i.e. the visual motion cortex in congenital nystagmus may display a variable excitability in accordance with how fast the eye is moving (the nystagmus is cyclic with phases of faster or slower eye movement). In summary, our data show that the brain is more flexible than previously thought in providing solutions for achieving visual perceptual stability in the face of continuous retinal image motion from a nystagmus.
We see patients with nystagmus due to multiple sclerosis, stroke or neurodegeneration who complain of seeing the visual world move. Our data in congenital nystagmus begs the questions as to whether a phasic modulation of brain activity can alleviate symptoms of seeing the visual world move in patients with symptomatic nystagmus.
Does dopamine D1 vs. D2 receptor modulation affect visual motion perceptual function? A potential approach to treating visual acuity problems in nystagmus.
Nystagmus patients complain of visual blurring since there is a continuous movement of the visual world across the retina. This loss of visual acuity can affect patients' ability to read, watch television or drive. A main reason for visual blurring in nystagmus is that the visual image spends little time on the most important part of the retina called the fovea. The fovea is that part of the eye with the highest resolution. The longer an image stays on the fovea the better we can see the detail. Conversely, if the image is only briefly viewed through the fovea, as occurs with nystagmus, then it is poorly seen. In effect nystagmus makes the visual image 'noisy' which makes it difficult for the brain to produce a clear image.
If however, we can improve the ability of the brain to extract visual detail when the visual image stays on the retina for only a brief moment then we may be able to improve the visual acuity of patients with a nystagmus. We modelled injecting neural nosie in visual motion brain areas by briefly applying non-invasive brain stimulation (called 'TMS' or Transcranial Magnetic Stimulation) when volunteers tried to look at a moving visual target. TMS, by adding nosie to the visual system, impairs the ability for subjects to detect the direction of visual motion, but only when TMS and the visual target are presented at the same time. We compared the ability of placebo versus two different dopaminergic drugs, cabergoline and pergolide, to modulate the effect of increasing neural noise injected by the TMS on visual perceptual performance. We did this using a double-blinded, Williams design cross-over study and found that pergolide but not cabergoline or placebo, protected against the disruptive effects of visual cortex TMS upon visual motion perceptual performance. This implies that dopamine D1 (but not D2) receptor activation may improve visual perceptual performance. We will test the effect of dopamine D1 receptor modulation upon visual perceptual performance in those patients with nystagmus whose main complaint is impaired visual acuity (as opposed to patients whose main complaint is of visual world motion or 'oscillopsia).
Our goal is to utilise a knowledge of the brain mechanisms of plasticity to help improve treatment, not just for patients with vestibular or eye movement problems but also for those with chronic neurological conditions such as traumatic brain injury, stroke or multiple sclerosis. We aim to use adjuvant therapy such as brain stimulation and drugs, to enhance plastic change and hence speed recovery with physical and cognitive therapy.
et al., 2016, Temporoparietal encoding of space and time during vestibular-guided orientation, Brain, Vol:139, ISSN:0006-8950, Pages:392-403
et al., 2015, The Neuroanatomical Correlates of Training-Related Perceptuo-Reflex Uncoupling in Dancers, Cerebral Cortex, Vol:25, ISSN:1047-3211, Pages:554-562
et al., 2013, Vestibular Activation Differentially Modulates Human Early Visual Cortex and V5/MT Excitability and Response Entropy, Cerebral Cortex, Vol:23, ISSN:1047-3211, Pages:12-+
Seemungal BM, 2007, Neuro-otological emergencies, Current Opinion in Neurology, Vol:20, ISSN:1350-7540, Pages:32-39
Guzman-Lopez J, Silvanto J, Seemungal BM, 2011, Visual motion adaptation increases the susceptibility of area V5/MT to phosphene induction by transcranial magnetic stimulation, Clinical Neurophysiology, Vol:122, ISSN:1388-2457, Pages:1951-1955